Pain: Is it good or bad? My answer is Yes, thanks to pain our body is able to understand that something is wrong with the painful area.

1. -Dr. Aniruddha Barot (PT)
B.P.T., M.P.T. (Musculoskeletal), C.K.T.T.
Assistant Professor
SKUM college of Physiotherapy
1

2. • What is Pain ?
• Types of pain
• Neurophysiology of pain
Pain pathways
• Neuromodulation of pain
• Pain modulation theories
• References
2

3. • The experience of pain results from a
physiological response to a noxious stimulus.
• It is subjected to a wide range of influences
& therefore, there is considerable variation
in the perception of pain between
individuals.
• These influences include: cultural
differences, states of emotion & past
experiences.
3

4. • Basic 2 types: ACUTE & CHRONIC.
• Acute pain:
With acute pain the body is responding to a noxious stimulus, which has caused the
damage, therefore the body’s protective mechanism is activated & the symptoms
reflect the underlying pathology.
The signs & symptoms of inflammation are very strongly perceived by the subject.
Pain is very intense.
• Chronic pain:
Typically, the original pathology is healed, so the symptom-pathology relationship is
not as straight forward as before.
The signs & symptoms of inflammation is considerably less.
The subject feels mild pain in certain activities.
4

5. • It should be understood, that there is no rigid pathway which is responsible for
the perception of pain; rather a multidimensional anatomical & physiological
system is involved, which takes a number of subjective factors into consideration.
• Physiologists use the term “NOCICEPTION” to describe the specific response to a
noxious stimulus, i.e. the transmission of noxious signal from the periphery to
cortex.
5

6. 1. Receptors
2. Afferent fibers
3. Dorsal horn
4. Spinal tract
5. Second order neuron
6. Thalamus
7. Cortex
6

7.  The receptors which responds to noxious stimuli –Nociceptor
 Latin word nocere- to injure.
 3 types-1) Mechanical
2) Thermal
3) Polymodal
 Activation of nociceptors is through release of certain chemical substance from the
damaged tissue / nerve terminals (Bradykinin, sub–p, serotonin).
 Once these chemicals are released – cause disturbance in membrane potential.
This in turn will initiate an action potential at the nociceptor – afferent fiber
junction.
 Once this AP initiated ,so start of activity in ascending nociceptive pathway.
7

8. 8

9. AFFERENT FIBERS
 1st order neuron:- starts at-peripheral receptor
ends at- dorsal horn of spinal cord.
 2nd order neuron: starts at- dorsal horn of spinal cord
ends at-thalamus.
 3rd order neuron:- starts at-thalamus
ends at- sensory cortex.
9

10. DORSAL HORN
 The cell bodies of group 3(Aδ) & group 4(C) fibers lie in the dorsal root ganglia of
the spinal cord.
 The central portion of these fibers enter the spinal cord in the lateral division of
the dorsal root.
 These fibers occupy the medial portion of the Lissauer’s tract; they bifurcate into
ascending & descending branches which may travel for one to three segments
before the synapse with second order neurons in the dorsal horn.
 Substance P is believed to be the neurotransmitter involved at the synapse
between first & second order neurons.
 The incoming group 3 & 4 fibers synapse mainly in laminae 1,2,3 & 5.
 Once they have synapsed, the second order neurons then cross to the opposite side
of the spinal cord & ascend in one of the two central pathways.
10

11. 11
DORSAL HORN

12. SPINAL TRACT (PATHWAYS)
 Though, there exists a multitude of names for the ascending tracts that carry the
second order nociceptive neurons, the 2 central pathways concerned with nociception
are the Lateral spinothalamic tract (LST) & multi synaptic ascending system (MAS).
 LST:
This tract contains the 2nd order neurons from the group 3(Aδ) fibers & thus carries the
fast, sharp type of pain.
The 2nd order neurons in this tract end in thalamus where they synapse with nuclei of
the venterobasal complex.
 MAS:
As the name suggest this is a diffuse system, of many collaterals & relays throughout
the brainstem.
It carries the 2nd order neurons from the group 4(C) fibers & subsequently it carries the
slow, burning, aching pain.
The MAS 2nd order neurons end by synapsing with the medial & intralaminar thalamic
nuclei.
12

13. SECOND ORDER
NEURONS
 These are of 2 types: Nociceptive specific neurons (laminae 1 of
dorsal horn) & wide dynamic range neurons (laminae 5).
13

14. BRAINSTEM STRUCTURE
 The structures involved include:
1.Reticular formation: it is a diffuse network of neurons which
extends from the medulla below to the thalamus above. It is
responsible for maintaining a state of alertness or awareness in the
brain.
2.Periaqueductal grey matter(PAG) & Nucleus raphe magnus(NRM):
These two are important structures which play a role in the
descending pain suppression system & opioid analgesia.
14

15. THALAMUS
 This important structure acts as a relay station for the most types of
sensation.
 At this stage of the ascending nociceptive pathways, nociception
reaches the level of consciousness.
 The 2nd order neurons which travelled in the two aforementioned
spinal pathways terminate here in the venterobasal, medial &
intralaminar nuclei.
15

16. CEREBRAL CORTEX
 The final destination for nociception & indeed all sensation is the
somatosensory cortex, which is located in the post-central gyrus of
the parietal lobe of the cerebral cortex.
 Here, the perception & interpretation of sensation occurs.
 The somatosensory cortex defines the intensity, type & the location
of the sensation (pain).
 The limbic system, which consists of a number of interconnected
structures, is located deep in the cerebral hemispheres.
 The limbic system, is believed to play a role in emotional aspect of
pain.
16

17.  The passage of nociceptive information can be interrupted along
several stages, along the ascending nociceptive pathways to produce
neuromodulation of pain.
 The ascending pathways to produce neuromodulation of pain
include:
1.Peripheral
2.Spinal segmental
3.Supraspinal
4.Cortical.
17

18. 18

19. Peripheral:
At this stage intervention involves a reduction in the amount of those chemicals
released in response to tissue damage which are responsible for nociceptor
activation.
Application of heat (SWD, Hot packs) to produce local vasodilatation will increase
blood flow to the affected area & in turn assist in removal of these chemicals.
Other modalities include, US can affect cell permeability & thus reduce the
amount of exudates formed in the inflammatory reaction.
The pressure of the exudates upon the nociceptors can initiate activity in the
nociceptive pathways which can be relieved by the application of ice immediately
after the injury.
19

20. Spinal segmental:
Intervention at this stage involves inhibition of activity in the small diameter
group 3(Aδ)& group 4(C) fibers before the incoming information ascends further in
neural axis.
Example: “Pain gate theory” described by Melzack & Wall.
Modalities working at this level: TENS, IFT, massage & vibration
Supraspinal:
The ascending pathways make imp synaptic connections with several brain stem
structures involved with descending pain modulations system as explained by
Melzack & Wall.
The placebo effect & counter irritation are also believed to operate at this level.
Modalities working at this level: UVR, Low TENS, Acupuncture
20

21. Cortical level:
At this level, intervention involves modification of individual perception &
interpretation of pain.
Example: Behavior modification & cognitive strategies.
21

22. 22
1
•Physiological blocking effect
2
•Pain gate theory
3
•Descending pain suppression system

23.  The effect observed is believed to block activity primarily in the nociceptive fibers.
 Thus, it has been referred to as a peripheral blockade of incoming nociceptive
signals.
 The reason behind is that the volume of nociceptive traffic is reduced, which will
in turn reduce the overall pain perception.
 After many studies it is concluded that application of high frequency electrical
currents over a peripheral nerve reduces the conduction velocity of nerve.
 Walmsley et al, conducted a study & they observed that application of TENS over
median nerve for 30 minutes, led to decrease in nerve conduction velocity of
afferent fibers.
23

24.  Gate control theory was described by Melzack & Wall.
 Basic concept is that, stimulation of large diameter fibers could reduce the
perception of pain which resulted from activity in small diameter fibers.
 Physiological gating mechanism exists in the dorsal horn of spinal cord; which
may allow/inhibit nociceptive traffic to proceed centrally.
The T cell is believed to be a wide dynamic range type of 2nd order neuron, found in
lamina 5 of dorsal horn, which act as a relay cell for ascending pathways.
Substantia gelatinosa (lamina 2 & 3) in spinal dorsal horn contains the gate.
24

25. It has an inhibitory effect on the terminals of group 2, 3 & 4 fibers which synapse with T
cell.
The small diameter group 3 & 4 fibers send an inhibitory collateral & large diameter fiber
send an excitatory collateral.
Afferent information travelling to group 2 fibers will serve to increase the inhibitory effect
of S.G. upon T cells.
& therefore, closes the gate to nociceptive traffic.
Activity in small diameter fibers, reduces the inhibitory effect of S.G. over T cells
And thus the gate remains open & nociceptive traffic can proceed
25

26. 26

27.  DPSS is a 3 tiered anatomical system, which has the following
components:
1.The Periaqueductal grey matter (PAG)
2. The Rostral ventral medulla (RVM) [Nucleus Raphe Magnus &
adjacent reticular nuclei]
3.The Spinal dorsal horn
27

28. The activation of Aδ pain fibers may provoke impulses in the midbrain that then
travel back down the spinal cord to inhibit nociceptor neurons at the original level.
The Aδ nociceptors in the spinothalamic tract give off collateral branches to the PAG
in the mid brain.
Descending neurons from this region pass to various sub regions of the RVM & then
to the spinal cord dorsal horn generating encephalin in the S.G.
These & other known descending pain suppressing pathways use serotonin & nor-
adrenaline as neurotransmitters.
28

29. Endogenous opioids are also released at both brain stem & spinal cord levels
The net effect of opioid release at the level of PAG & NRM is activation of descending
projection neurons
Stimulation of PAG by ascending fibers causes the release of opioids & it is believed
that the opioids released at this level have the effect of inhibiting an inhibitory
interneuron thereby excite the descending pathways to the NRM.
The RVM which receives afferents from serotonin & neurotensin containing neurons,
project to the spinal cord dorsal horn via the dorsolateral funiculus, where the
released opioids have inhibitory effects.
29

30. Opioids bind to pre-synaptic
receptor site on substance P
containing nociceptive afferents
And thus inhibit the release of
substance P; as substance P is a
neurotransmitter necessary for
nociceptive transmission
& this leads to inhibition of pain at
the spinal cord level
30

31. 1.Low & Reed. Electrotherapy explained. 4th edition.
Elsevier publications.
2.B Nanda. Electrotherapy simplified.1st edition. Jaypee
publications.
31

32. 32